HLTH 4150 Test #1 Study Guide 1. Body Mass Index (BMI

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HLTH 4150 Test #1 Study Guide
1. Body Mass Index (BMI)– indicator of body fatness; weight (kgm)/height (cm)2
Percent Body Fat– percentage of fat your body contains, including essential body
fat and storage body fat
Waist Circumference– numerical measurement of your waist; fat around the waist
increases the risk of obesity-related health problems
Hypothalamus– part of the brain that releases hormones which control the
function of the pituitary gland, as well as messages among the gut, fat cells and the
brain
 Blood nutrients, hormones, and neural signals (the way food looks and
tastes to us)
 When stimulated, the hypothalamus can promote fat and carbohydrate
intake and storage, as well as lower metabolism to conserve energy
(increasing hunger)
Homeostasis– process by which a steady state of equilibrium in the body with
respect to physiological functions and chemical compositions of fluids and tissues is
maintained
 The role of the hypothalamus in regulation of homeostasis is essential for
survival; the hypothalamus uses a set point to regulate the boy’s systems
Prevalence– proportion of individuals in a population having a disease or
characteristic
Mortality– the number of deaths in a given time or place; mortality rate
Morbidity– the incidence of disease; the rate of sickness
Risk Rates–
Adipocytes– cells that primarily compose adipose tissue, specialized in storing
energy as fat; ~80% and 20% water; Triglycerides are the main storage form of fat
energy
Brown Fat (BAT)– makes up 1-3% of total fat, has a much higher number of
mitochondria which make it brown and has more capillaries because it has a greater
need for O2 than most tissues; children and hibernating animals have more brown
fat than adults and is found in the neck, upper back and around the collarbones
 Stimulated by increased carbohydrate intake; burns calories to generate
heat
 Composed of several small lipid droplets and a large number of
mitochondria
White Fat (WAT)– much more plentiful than brown fat; stores energy and produces
hormones that are secreted into the bloodstream; it is also a thermal insulator and
cushion for our internal organs
 Produces leptin as well as receptors for insulin
 In women it accumulates around the hips, thighs, butt and breasts, while it
accumulates in the belly for men
Fat-free Mass– mass comprised of the nonfat components of the human body (ex:
skeletal muscle, bone and water)
Hypertrophy– increase in the size of an organ or tissue due to the enlargement of
its component cells, in this case fat cells
Hyperplasia– increased cell production in a normal tissue or organ, in this case fat
cells
 In hypertrophic obesity, there is a greater number of fat cells that are also
larger than normal; begins at an early age
Resting Metabolic Rate (RMR)– the energy required to perform vital body
functions such as respiration and heart rate while the body is at rest (60-70% of
ones daily energy expenditure); less rigorous measure than Basal Metabolic rate
Thermic Effect of Food (TEF)– the energy expended by our bodies in order to
consume (bite, chew and swallow) and process (digest, transport, metabolize and
store) food; carbohydrates are more likely to be expended as energy (heat) because
it is not a preferred fat energy storage source
Thermic Effect on Exercise (TEE)– the energy expended during an activity in
excess of that required for resting metabolism; 20-30% of daily energy expenditure
NEAT– “Non-Exercise Activity Thermogenesis”; the energy expended for everything
that is not eating, sleeping, or pointed exercise; such as chores, work related tasks,
fidgeting, and walking as a mode of transportation
Energy Expenditure– the sum of the basal metabolic rate (resting metabolic rate),
the thermic effect of food, and the thermal effect of exercise
Genotype– the genes that an organism carries
Phenotype– observable characteristics
Heritability and Obesity– Heritability is the fraction of the population variation in
a trait that can be explained by genetic transmission; estimates can be inflated when
there is little environmental variation; twin studies, adoption studies and overeating
studies
 Heritability of BMI is 25-40%
 Heritability of subcutaneous fat is 30-50%
 Heritability of regional fat distribution is 40%
Thrifty Genotype– theoretical genotype thought to occur in populations that
developed in unique environments; adapted to survive harsh environments with a
very efficient metabolism, however when in a western world with a western
environment, their genotype actually makes them more vulnerable to obesity ex:
Pima Indians
Constitutional Thinness– unique trait thought to confer resistance to the
development of obesity even in an obesogenic environment
Central Factors– Pons- midbrain and thalamus (sensory properties of food),
hypothalamus, and nucleus accumbens, amygdala and frontal cortex
(preference/aversion)
Peripheral Factors– Macronutrient quantity/quality (important role in
determining diet’s behavioral and metabolic consequences), neurotransmitters
(dysfunction), neuropeptides, hormones, and receptors
 Macronutrient= proteins, carbohydrates and fats
 Neurotransmitter= chemical that modifies or results in the transmission of
nerve impulses across synapses
 Neuropeptide= slow acting transmitters, longer lasting, made by nerve cell
body
Cholecystokinin (CCK)– released by the GI tract, stimulates the vagus nerve to
terminate eating (promotes satiety)
Neuropeptide Y– released when carbohydrate stores are low; signals the brain to
begin eating; leptin reduces output of NPY. NPY blocks leptin
Melanocortin-4– protein in humans that has been found to be involved in feeding
behavior, the regulation of metabolism, and sexual behavior
Insulin– released from the pancreas especially when a meal is high in
carbohydrates, promotes glucose uptake, fat storage, and meal termination
(promotes satiety); rises in response to increased blood glucose levels
Insulin Resistance– cells of the body become resistant to the hormone insulin, so
higher levels of insulin are needed in order it to have its proper effects so the
pancreas produces more insulin
 Insulin resistance in fat cells reduces the normal effects of insulin on lipids
(fats) and results in reduced uptake of circulating lipids, elevating fat levels
in the blood plasma
Acanthosis– thickening of the skin usually found in body folds such as the neck,
armpits, groin, navel, and forehead; in obese individuals it is most likely because of
insulin resistance
Leptin– “satiety hormone”, activates hormone that we feel good and depresses
chemicals in charge of hunger; regulates the amount of fat stored in the body by
adjusting the sensation of hunger and adjusting the energy expenditures, hunger is
inhibited when the amount of fat stored reaches a certain level; high fat diets inhibit
leptin activity!
Leptin Resistance– elevated leptin levels fail to control hunger and modulate
weight; there can be high amounts of leptin circulating in the blood but the body
does not respond to it, possibly because the leptin receptors stop functioning
properly
Cortisol– released by the adrenal glands; steroid hormone, stress hormone;
promote fat intake and fat storage, especially in the abdomen; fat cells convert
cortisol from its inactive to its active form
 Stress compounds- high stress environments and a certain diet can cause
someone to gain more fat than if they were in a lower stress environment
Adiponectin– produced by fat cells, counters the effects of resistin (causes high
levels of LDL); reduced inflammation, improves insulin sensitivity, improves lipid
ratios; decreases with increasing fat cell size
Resistin– also produced by fat cells; promotes FA which increases the release of
glucose by the liver (increasing blood glucose levels); helps during starvation, but is
bad for diabetics because it promotes insulin resistance
Lipoprotein Lipase– also produced by fat cells; enzyme that brings fat into the cell;
the bigger the cell, the more enzyme it produces so it brings in more fat
 Peripheral/subcutaneous fat is less metabolically active, but higher
lipoprotein lipase activity
Compression of Morbidity (in relation to obesity)– try to delay the onset of illness
for as long as possible so that the illness is limited to the last few (or less) years of
life; increase quality of lifespan and decrease time suffering
Satiety factor– satiety= the state or quality of being fed or gratified to or beyond
capacity; the inhibition of hunger and further eating that arises because of food
ingestion
Lipostat– model proposes that adipose tissue (fat reserves) is directly involved in
the hormonal regulation of appetite and energy expenditure
Parabiosis– two mice are sutured together to make a parabiotic pair in which their
vascular systems are united; found the idea that a satiety hormone (leptin) is
produced in the hypothalamus and suppresses hunger
Ecological fallacy– make assumptions on individuals based on group data ex: BMI
Exceptional fallacy– take data about an individual and make assumptions about a
group
Correlation vs. Cause– correlation= relationship between two or more things
which change; causation= cause and effect relationship between variables
Principle of Equifinality– how different early experiences in life can lead to similar
outcomes (different ways to get an outcome)
Metabolism– metabolism is a collection of chemical reactions that take place in the
body’s cells, converting food we eat into energy needed
 Factors increasing metabolism include: increase in muscle mass, physical
fitness, male gender, hyperthyroidism, pregnancy, puberty, extremes in
environmental temperatures, caffeine, smoking (3-5% increase), and fever
(7% increase for every 1 degree F increase)
 Factors decreasing metabolism include: decrease in lean tissue, poor
physical fitness, female gender, under nutrition, hypothyroidism, sleep (10%
decrease), aging (3-5% decrease per decade after 25 years of age), and
weight that is below set point
Weight regulation– “fat regulation”; there are two ways to regulate weight:
1) Appetite/feeding, and 2) Metabolism
 Short-term feeding: day-to day intake, lots of thing influencing it
 Long-term feeding: tied to our fat stores
 In pre-puberty animals and humans, appetite is characterized by a
stronger preference for carbs in females and for protein in males
Reduced Obese– individuals who have lost large amounts of weight; some studies
show a reduced energy expenditure, while other studies show a normal change in
energy expenditure; people who used to be obese require a smaller calorie intake
than lean individuals; might need higher levels of physical activity to maintain their
weight loss
Restrained Eater– don’t let themselves eat what they want or are always watching
what they eat; when they do give in and eat what they want it is usually out of
control eating
Preload– a meal/drink given before an experiment
Disinhibition– person loses control and overeats as a response to the environment
(i.e. availability, emotional stress, social gatherings); obesity has been associated
with disinhibiting eating
Set Point– weight range your body is programmed at and will fight to maintain it
when weight changes from the set point; 10% variations in weight (up or down)
trigger the body to adapt back to the set point; controlled by metabolism
 Set Point Theory: proposes that body weight regulation is controlled by
the regulatory center of the hypothalamus; set point can change with
persistent pressure
Asymmetrical Quality of Weight regulation– there is a preference for weight gain
over loss
Central Adiposity– accumulation of fat resulting in an increase in waist size;
visceral fat is packed between internal organs and torso and is composed of white
adipose tissue; increased risk of cardio-metabolic disorders! Android fat
distribution is the distribution of adipose tissue mainly around the trunk and upper
body such as the abdomen, chest, shoulder and nape of neck and is also associated
with higher risks of coronary artery disease; significant correlation with metabolic
syndrome; more common in men
 Measured as increase in waist circumference or waist-hip ratio
Peripheral Adiposity– associated with less-severe health risks; gynoid fat
accumulates on the hips, thighs and buttocks; non significant correlation with
metabolic syndrome; more common in women
PPAR trio– fat cells, regulate lipolysis and storage
 PPAR gamma– fat storage, expressed in adipose tissue; sensor for dietary
fat, master regulator, regulates insulin resistance, glucose gridlock
 PPAR delta– fat burning, expressed in muscle
 PPAR alpha– fat burning, expressed in liver
Glucose Gridlock– interferes with the insulin's ability to communicate with the
cell’s surface, so the glucose begins to build up sending out signals to the body that
we need more insulin (however the body doesn’t know that the insulin isn’t
responding)
Metabolic Syndrome (Syndrome X)– really important area! Suggests that for
certain people with obesity, they have a metabolic response where the health affect
is greater than the sum of the parts= compound on each other and make their health
problems worse; risk factors!
Ob mutation mouse– eats excessively and becomes profoundly obese; led to the
discover of the hormone leptin
Db mutation mouse– the mouse got fat, and were diabetic and the islets of
Langerhans were abnormal; leptin receptor activity is deficient
Black-6 db–2J mouse– ate a lot, gained weight, and had high levels of insulin in the
first few months of life, but as they aged they continued to get fatter and fatter yet
never developed full-blown diabetes
Black-Kaliss db–2J mouse–overate, became fat, had high levels of insulin,
developed diabetes at a young age, and died
 db-2J mutation behaved like diabetes in the Black-Kaliss mice, but like
obese when in the Black-6 mice
 ob mutation behaved exactly the same way
Macronutrients– protein, carbohydrate and fat; needed for growth, metabolism,
and other body functions; provide energy; carbs and proteins both provide 4
calories per gram, while fats provide 9 calories per gram (more energy)
 Polyunsaturated and monounsaturated fats– provide important metabolic
regulation information to the body
 Saturated and trans-fats– do NOT provide important metabolic regulation
information to the body; don’t bind well with PPAR fat receptors and don’t
help with metabolic regulation; EASIER TO STORE
Bogalusa Heart Study– long-term population study; studied atherosclerosis,
coronary artery disease, and hypertension in children and adults from birth to age
45; have found that:
 atherosclerosis and high blood pressure start at an early age
 environmental factors are significant and influence high cholesterol, high
blood pressure, and obesity
 obese children will likely be obese adults, and have hardened arteries at
about age 30
Ecological Model–
Public Policy– media/advertisement, development, food pricing
Community– SES characteristics, built environment, access to parks/gyms
Organization– school/workplace food, food availability
Interpersonal– screen time, social support, culture, food availability at home
Intrapersonal– preferences, motivation, health status, self-confidence, perceptions
Fatty Liver Disease– liver enlarges over time and liver cells are replaced by scar
tissue, the liver doesn’t work right and develop liver failure, liver cancer and liverrelated death
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